6.4

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Because back pain is a self-limiting disease in the majority of cases and its prevalence is so high, imaging of every patient with complaint would be very costly.

Back pain does not follow the classic model of disease, in which symptoms closely correlate with imaging abnormalities. For example, roughly 80% of patients with low back pain may have no detectable abnormalities.

Asymptomatic individuals, however, may be found to have striking findings on imaging studies. In many cases, radiology will serve only to rule out other serious conditions (such as neoplasm or infection), for accurate localization of disk herniation, and for surgical plan- ning.

Spinal Degeneration Pathophysiology

The disk consists of the annulus fibrosus, nucleus pulposus and porous, cartilaginous endplates (Fig. 1). It is an osmotic system, in which proteoglycans bind “free”

water. The nucleus has a very high expansion power (6–8 atm osmotic swelling pressure) (Fig. 2). During Introduction

Back pain and spinal diseases are the second most common problem that prompts patients to visit physicians.

The increase in back disabilities surpassed all other cases tenfold between 1980 and 1990. In the same period, conventional radiography, bone scintigraphy, myelography and discography were supplemented by CT and MRI. In the last years PET was added. The wise use of all these different modalities is a great challenge.

Chapter

Contents

Introduction . . . 703

Spinal Degeneration . . . 703

Pathophysiology . . . 703

Imaging . . . 709

Inflammation . . . 715

Pathophysiology . . . 715

Imaging . . . 716

References . . . 719

Nonneoplastic Disease 6.4

of the Spine

Herwig Imhof

Fig. 1.Schematic drawing: lateral view of spine with disk, showing the nucleus pul- posus (x), annulus fibrosus (arrowhead) and cartilaginous endplates (arrow)

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motion the normal eccentrically located nucleus pulposus seems to migrate anteriorly and posteriorly. During extension a posterior disk bulge is greatest. During re- laxation the disk takes up water and attains its full size (preloading). This full-size disk stretches the accompanying ligaments (anterior and posterior longitudinal ligaments, etc.). Therefore the spine is an elastic rod.

Loading of the spine leads to an elastic deformity of the spine, strengthening its physiological S-shaped lordosis and kyphosis [1–3].

During loading the disk becomes dehydrated, caus- ing the accompanying ligaments to become loosened.

The disk-height is reduced. The spine loses its homoge- nous elasticity. In turn, localized overloading of the disk and subchondral spinal endplates may take place.

The disk is only partially vascularized until the age of 4 years. Later on nourishment is based on fluid diffusion from the neighboring bony endplates and soft tissue (ligaments, etc.) (Fig. 3). Diffusion is enhanced by motion. Lack of motion over a long period of time leads to metabolic problems and inadequate nutrition. The fre- quency of this motion is also very important. Whole- body vibration frequencies of about 4–5 Hz may result in fluid stasis and metabolic problems within the disk [4].

Recurrent localized overloading – particularly in the lower lumbar and cervical spine – leads to tears in the annulus fibrosus (Fig. 4). The expansion power presses nucleus pulposus masses into these tears (internal disruption). In the worst case it leads to herniation, which could be either protrusion of nucleus material (with or without preservation of the overlying longitudinal structures) or disk extrusion (with obliteration of the overlying longitudinal structures). A herniation does not inevitably result in neurological symptoms. On the contrary, it is assumed that in older age groups (>50 years) the majority of disk herniations occur without any clinical symptoms. Moreover, it is well known that there may be a repair mechanism by fibrovascular tissue, which dissolves the protruded disk within 9–12 months. For this reason, among other things, without corresponding clinical symptoms the treatment of herniated disks is very conservative nowadays. The coming and going of disk herniations during life may represent the natural life of disks. Only in relatively rare cases they will develop clinical signs. On the other hand, in some cases the herniated disk loses the connection to the central part completely and shifts independently up – or downwards – in the spinal canal (sequestered disk) [5].

As a result of degenerative processes, tiny calcifications may develop within the disk (Fig. 5). As a sign of internal structure disruption with dissolution of gas Fig. 2.Vertebral disk specimen: swelling of the disk due to the os-

motic swelling pressure of the proteoglycans

Fig. 3.Schematic drawing: compression and decompression of the disk with exchange of metabolic products during motion

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(nitrogen) the so-called vacuum-phenomenon may be recognized [6].

A process very similar to that described in the anteri- or and posterior part of the disk may take place within the bony endplates. If these and the annulus fibers are

weakened locally (e.g., in osteoporosis) the nucleus pulposus, because of its high internal pressure, will invade the bone resembling Schmorl’s node. Active (symptomatic) Schmorl’s node shows signs of inflammation and fracture healing (Fig. 6).

Fig. 4.Micromorphological sagittal cut with HE staining of a protruded disk with tears within the annulus fibrosus and nucleus pulposus

Fig. 5.Macromorphological sagittal cut of a lumbar spine specimen: calcification within the annulus and dorsal longitudinal ligament (chondrocalcinosis); minor dorsal herniation

Fig. 6.Macromorphological sagittal cut of a lumbar spine specimen: herniation of disk tissue into the neighboring bone (Schmorl’s nodes). The herniation is surrounded by sclerotic bone

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Since the introduction of MRI into routine clinical imaging it has become well known that there are also degenerative changes within the bony endplates. Just as in synovial joints, this border region is damaged during overloading. This results probably in pain and activation of fibrovascular tissue, producing a pseudoinflammatory state representing stage I (Modic) degeneration.

Today, it is assumed that the endplate fails before the in- jured annulus fails. Endplate failure seems to be the pre- cursor to disk degeneration, since failure may disrupt disk nutritional pathways from the vertebra. Later on, this recurrent damages (stress) to the endplates leads to

localized fatty conversion (stage II) (Fig. 7). Stage III is represented by the well-known subchondral calcifications (sclerosis). In Stages II and III the exchange of nu- trients is increasingly reduced because of the further loss of fine vessels and endplate calcifications. The num- ber of chondrocytes that support the disk will be diminished [1, 7].

As a side effect, it must be noted that the activated fibrovascular tissue of the endplates and surrounding soft tissue may grow into the disk, ending in neovascu- larization of the disk, particularly at the anterior and posterior part (Fig. 8).

Fig. 7.Macromorphological sagittal cut of a lumbar spine specimen: high-grade os- teochondrosis with a central tear and fatty marry conversion, subchondrally

Fig. 8.Microscopic cut with Gieson staining: capillary invasion into the annulus fibers (revascularization of the disk)

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During aging and degeneration the disk loses water.

A healthy disk contains approximately 85% water, the rest being collagen and proteoglycans. Whether aging and degeneration are the same pathophysiological process is still unclear. However, there is no question that degeneration is mostly found in the aged population [8]. Given the loss of water in aging and degeneration, the water content drops to approximately 70%. The disk becomes more fibrous and disorganized, with loss of distinction between nucleus and annulus; the preloading of the accompanying ligaments is minor. While in the healthy, young spine loading takes place in the central part of the disk, this loading process is shifted pe- ripherally to the annulus fibers in the chronically over- loaded spine, leading to the above-described tears in the annulus. The spine as a whole becomes less elastic, the ligaments are looser. Local instability may develop, best visualized by in increasing retrolisthesis and spinal stenosis (Fig. 9). Local stress on the ligaments and instability itself leads to the formation of (traction) osteophytes. These prevent stress by restricting movement and restoring stability.

Following vascular invasion, progressive breakdown of the disk-tissue contents will result in their resorption. At this stage, the narrow space between the vertebral bodies will be occupied by a small amount of vascularized fibrous tissue, the neighboring bone becomes sclerotic. Frequently, the final stage of the resorption process is the spontaneous fusion of adjacent vertebral bodies (Fig. 10).

The intervertebral (facet) joints are typical synovial joints. They normally have a very thin corticalis laterally, which may even vanish in older people. Their degenerative changes are the same as in any other joint: cartilaginous and subchondral changes leading to cartilage edema, fibrillation and localized baldness, subchondral edema, cysts, sclerosis and effusion osteophytes and joint-space narrowing as well. A very typical marker for degenerative changes are synovial cysts. The innerva- tion of the facet capsules is very rich. The angulation of the facet joints seems to be very important for the devel- opment of degeneration. The 3D orientation of the facet joint surfaces shows a gradual and characteristic change through each of the cervical, thoracic and lumbar spine regions. The kinematic constraints provided by the facet joints are particularly pronounced in the cervical spine, where there is marked coupling between lateral bending and axial torsion. In the thoracic spine they are organized like segmental socket joints. In the lumbar spine there is a great variation in the 3D orientation

Fig. 9.Macromorphological sagittal cut of the lumbar spine: degenerative spondylolisthesis at L3/L4 with disk-space narrowing and a step formation between L3 and L4. Schmorl’s node at L2

Fig. 10.Macerated lumbar spine (sagittal cut): bony fusion in se- verely degenerated disk

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between sagittal and coronal orientation. While in the majority of cases, L1/L2 is more sagittally oriented, L4/L5 is in almost 90% frontally oriented: the former limits axial rotation, the latter flexion. It must be stressed that the surface of the facet joints is almost nev- er flat, but arcuate (Fig. 11). Accordingly, the possible overloading depends in part on the positioning and surface of the facet joints. This is even aggravated if there is a asymmetry in the facet-plane orientation (tropism), which is found in approximately 30% of men and wom- en. In such cases with a tropism of more than 5°, invari- ably a local overloading will take place during rotation (Fig. 12). It is therefore not surprising that in such cases annulus fissures are found unilaterally in 80% of all cases [4, 9, 10].

Facet joints and the disk share the load. In an upright position, 80% of the load is taken by the disk, 20% by the facet joint. In a flexed position the facet joint has to take over 50% of the load. The highest facet joint pressure develops under combined rotation, flexion, and compression. Reduction of disk height by 1 mm increases the facet-joint load by 36%, a 4-mm loss by 61%.

Spinal ligaments pass between each vertebra along the length of the spine and function to limit excessive joint motion. These ligaments include the anterior and posterior longitudinal ligaments, the ligamentum fla- vum, the inter- and so-called supraspinous ligaments, and the intratransverse ligaments. The facet-joint capsules and the annulus fibers also act as tension-bearing structures between the articular process. The anterior

Fig. 11.Macromorphological cut (axially) through the facet joints: asymmetry of the joint surface (tropism). On the left side the articular cartilage is rare- fied

Fig. 12.Schematic drawing of the spine (axially) during rotation to the left side:

there is a localized overloading in the right facet joint. The rotation is limited by the ligaments around the left facet joint and the annulus fibers

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longitudinal ligament is nonelastic and limits hyperex- tension and rotation. The posterior longitudinal ligament limits ventral flexion and lateral bending. The elastic flaval ligaments are very important for the preloading process and tend to calcify very early in life (Fig. 13). The interspinous ligaments limit ventral flexion and dorsal shifting. The so-called supraspinous ligament is actually not a ligament, but part of the fascia thoracolumbalis. The facet-joint capsules, particularly in the lumbar region limit shifting during rotation. All ligaments are extensively supplied by proprioceptors.

They probably allow a direct coordination (activation) of the back muscles [3].

One of the major clinical questions is why pain is ex- perienced in degenerative disease. Currently, it is thought that this is an acute decompensation in already damaged tissue. Critical points are possible bony ste- noses and ligament problems: spinal canal stenosis with disk protrusion or extrusion and foraminal stenosis with osteophytes (Fig. 14) . Ligament – and capsular – lesions (e.g., overstretching) cause pain in about 70% of all cases. Subchondral bone marrow changes may also lead to pain (e.g., edema). Finally, disk tears themselves may provoke pain (internal disruption of the disk) by cytokines and macrophages [7].

Imaging

The basic imaging procedures are still conventional radiographs in two planes.

The first signs of incipient degeneration may be localized malalignments (retrolisthesis) with or without rotation of the vertebral body. Functional images (ex- amination in maximal ante- and retroflexion or side- bending) can show abnormal localized mobility (Fig. 15). Later on, the disk spaces become narrowed (chondrosis) and subchondral sclerosis is seen (osteo- chondrosis) (Fig. 16). The disk height in the spine normally shows a progressive increase in height from crani- ally to caudally with the exception of C7/Th1 and L5/S1, which show normally a lower height than the vertebral body above. The facet joints also show narrowing and subchondral sclerosis with irregular surfaces. Osteoph- ytes may develop near the disk laterally and anteriorly, rarely posteriorly, and at the facet joints as well. They are also signs of segmental instability [5, 11].

Fig. 13.Axial specimen radiography of lumbar facet joints: degenerative joint space narrowing with osteophytes (arrows).

Typical calcification at the insertion of the left flaval ligament

Fig. 14.Lateral conventional radiograph of the cervical spine: disk space narrowing and dorsal osteophytes with foraminal stenosis (cranial arrow). The calcified band crossing the foramen is a nor- mal variation (caudal arrow)

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As degeneration progresses, the disk height becomes significantly diminished, osteophytes become prominent, and the motion segments (disk + two complete vertebrae) become stable, but less mobile.

Discrete abnormalities within the facet joints may be best evaluated with CT (Fig. 17). CT also allows recogni-

tion of disk calcifications (Fig. 18) and gas (vacuum phenomenon) within the disk. The latter is one of the best signs of degeneration on conventional radiographs; the former may be found in aging and degeneration, but also in metabolic diseases (e.g., pyrophos- phate disease, hyperparathyroidism, ochronosis, diffuse idiopathic skeletal hyperostosis, etc.).

Only in the lumbar spine is CT almost equal to MRI in visualization of disk bulging and herniation (protrusion and extrusion) (Fig. 19) [4]. A protrusion is a local- Fig. 15.Functional conventional radio-

graphs of the cervical spine in maximal retro- and anteflexion: uniform and har- monious (smooth) flexion in all segments.

The three lines (anterior vertebral body line, posterior vertebral body line, inter- laminar junction line ) must run parallel.

There should be a tiling up of the vertebral bodies

Fig. 16.Lateral conventional radiograph of the lumbar spine: oste- ochondrosis L5/S1 with disk space narrowing, subchondral sclerosis, and anterior osteophytes

Fig. 17.Axial CT of the lumbar spine: severe degenerative changes in the facet joints with joint space narrowing, irregularity, osteophytes, and subchondral sclerosis. The angulations of the facet joints are asymmetrical (tropism)

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ized abnormality of disk contour wherein the base of the abnormality measured along the circumference of the disk is greater than the extension beyond the circumference, measured perpendicular to the base.An extrusion is a localized abnormality of disk contour wherein the base of abnormality is narrower than the extension beyond the circumference. A disk bulge is a generalized extension of the disk (at least 180°), usually limited to 3 mm [7].

It must be stressed that these definitions of protrusion, extrusion and bulge are strictly morphological, but pathoanatomically a bulge may have full-thickness annular fissures. Similarly, protrusions do not necessar- ily have intact outer annular fibers and extrusions may consist of a combination of nuclear and annular material. Clinically, there is in most cases no real relation between pain and morphology. Nevertheless, large com- pressive lesions (i.e., disk extrusions) are almost always symptomatic. The best surgical results are achieved when 1) a well-defined disorder is demonstrated by imaging studies and 2) imaging findings are closely corre- lated with the clinical history and physical findings.

CT directly outlines the herniated soft tissue masses, minimized epidural fat (lumbar spine) or subdural fluid space (cervical spine). It is important to distinguish far lateral from lateral and central extrusions, and calcified Fig. 18.Specimen lateral radiograph of the lumbar spine: disk cal-

cifications with minor degenerative abnormalities

Fig. 19. AAxial CT of the lumbar spine: right lateral disk prolapse with obliteration of the epidural fat, but no compression of the dural sac.BLateral MRI of the lumbar spine (spin density image):

protrusion of the disk dorsally L3/L4 with preservation of the longitudinal ligament. Compression of the dural sac. Disk-space narrowing and minor reactive fatty marrow conversion

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from uncalcified ones. The latter distinction may be particularly important before invasive treatment, since hard or calcified prolapses cannot dissolve. In some cases, the extruded disk loses its connection with the central part and becomes a sequestrum, which may move up or down in the spinal canal and be calcified or uncalcified (Fig. 20).

In the last few years, MRI has become the standard imaging method in many centers. It allows direct visualization of the disk itself. Because of its high water content, the nucleus pulposus is bright on T2-weighted images. With aging and degeneration, it gains a horizontal dark line (nucleus cleft), later becoming less bright until it reaches the same low intensity as the surrounding annulus fibrosus. Meanwhile, the size and height of the disk decline continuously (Fig. 21) [8, 12].

In acute stage I (Modic) the subchondral bone marrow and any active Schmorl’s nodes are hyperintense on T2-weighted images (Fig. 22) and enhance after intravenous injection of contrast medium (Fig. 23). Stage II shows fatty subchondral intensities (hyperintense on T1- and T2-weighting). Finally, sclerosis (stage III) will show a low intensity signal in all sequences.

Disk bulging or herniation is seen directly, as described above in the paragraph on CT. The sign is en- compassed by loss of epidural fat or subdural CSF

Fig. 20.Lateral MRI of the lumbar spine (spin density): low-density disk sequester at the height of the vertebral body L1

Fig. 21.Lateral T2-weighted MRI of the lumbar spine showing different stages of disk degeneration. Uppermost disk: disk has bright hyperintensity and a horizontal dark line (nucleus cleft). Middle disk: intensity of annulus fibrosus and nucleus pulposus is very low due to loss of water. The height of the disk is reduced. Lower- most disk: disk height is reduced, but there is still hyperintensity within the disk, probably also representing remaining expansion power

Fig. 22.Lateral T2-weighted MRI of the cervical spine showing stage I degeneration with subchondral bone marrow edema. In- dentation of the dural sac is visible, minor retrolisthesis. The patient has severe pain

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space, obliteration of the longitudinal ligaments, and thickened epidural veins (Fig. 24). Direct compression of the medulla or nerve roots can be visualized. The majority of herniated disks shrink by more than 75%. The shrinkage occurs in the 1st month after symptoms start, as a result of hydration followed by quick dehydration.

This process explains why some extruded disks appear bright on T2-weighted MR images early in the disease (Fig. 25). Only 8% of disk herniations enlarge. Extru- sions and large protrusions have the highest rate of spontaneous shrinkage and symptom improvement.

Internal disk disruption is a controversial entity, the proponents of which believe that chronic lumbar back pain originates in the disk. The mechanism is thought to be leakage of the nucleus pulposus into the outer annulus or epidural space without frank herniation.

Postoperatively, in 15% of all cases patients have the same symptoms as before (failed back surgery syndrome). In these cases, the question arises of whether there is a recurrent or residual disk herniation or only scarring. By intravenous injection of contrast medium, MRI (CT as well, in the lumbar spine) can differentiate between the two: even if the operation is years in the past, scar will show an enhancement due to fibrovascular tissue and have no mass effect, whereas recurrent or residual disk prolapse will reveal no enhancement, but typically a mass effect. In some cases a recurrent or residual disk may be surrounded by scar tissue (Fig. 26).

Epidural scarring is responsible for 24% of all failed back operations [14].

There is a high correlation between the extent of scarring and the severity of recurrent radicular pain.

Less common causes of failed back syndrome are postoperative diskitis, arachnoiditis and instability.

CT myelography and discography are rarely used nowadays. MRI should give the same results in the vast majority of cases. Only in cases of unexplained back pain where localization is impossible, examinations Fig. 23.Lateral T1-weighted MRI of the lumbar spine with contrast

enhancement showing subchondral and linear disk contrast en- hancement (arrows) due to (pseudoinflammatory) fibrovascular tissue in stage I degeneration (repair mechanism) with revascularization of the disk

Fig. 24A, B.Lateral T1-weighted MRI of the lumbar spine.ALateral:

dorsal disk herniation at L3/L4 with localized fatty marrow conversion. Severe disk space narrowing with fatty marrow conver-

sion at L5/S1.BAxial: left-sided low-intensity mass in the foramen representing a disk extrusion

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Fig. 26A, B.Postoperative axial T1-weighted MRI of the lumbar spine Abefore and Bafter injection of contrast medium.ALow-intensity mass within the left anterior epidural region. The nerve

root cannot be distinguished.BEnhancement of the low-intensity mass except for the swollen nerve. Arrow: scar tissue

Fig. 25. A Lateral T1-weighted MRI of the cervical spine: low-intensity disk extrusion at C4/C5 with impression of the dural sac (arrow).

BLateral T2-weighted MRI of the cervical spine: the disk material is hyperintense (arrow)

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with spinal loading may reveal hidden abnormalities.

Discography with pain-relieving drugs may discern symptomatic levels in cases of multiple-level disk disease.

Inflammation

Spondylitis is a rare disease, constituting only 1%–4% of all cases of osteomyelitis. It is more common in males (male:female ratio, 3:1). Typically, it is found in the older age group (60–80 years). Spondylitis is in most cases preceded by infections elsewhere in the body such as the respiratory system, genitourinary system, and the skin. Predisposing factors are diabetes mellitus, intravenous drug abuse, liver disease, kidney failure and conditions that suppress the immune system. Due to the in- sidious onset of the disease – particularly in granulomatous spondylitis – a delay in diagnosis is very common [13].

Pathophysiology

In the majority of cases the infectious process is trans- ferred hematogenously by arteries or veins, rarely by direct continuous invasion. In recent years, cases the post- traumatic (postoperative) etiology have been increasing due to interventional procedures. The venous propagation is based on a retrograde flow in valveless veins within the abdomen or thorax (Batson plexus). Retro- grade venous flow develops whenever the internal pressure within the thorax or abdomen is heightened [2].

Spondylitis can be divided into pyogenic and granulomatous. The most common isolated organism in pyo- genic spondylitis is – unchanged for decades – Staphy- lococcus aureus, which accounts for 42%–84% of infec- tions, followed by streptococcus, pseudomonas and Es- cherichia. In granulomatous spondylitis, the most fre- quently found causes are tuberculosis, fungi (histoplas- mosis, aspergillosis), leprosy and parasites.

As anywhere in the body, a bacterial or viral embolus reaches a highly vascularized region where there is a local insult or immunosuppression (e.g., due to a microin- farction, trauma, etc.). Therefore the location of spondylitis is primarily based on vascularization, which is age-dependent. Until the age of 4 years, there are no end arteries in the vertebral body, only in the disk. Therefore newborns and children up to 4 years of age may primarily get diskitis. Older age groups have equatorial and metaphyseal end arteries, in which inflammation usually starts (Fig. 27). The infectious process is therefore located anteriorly, near the disk or centrally in the vertebral body. It may include the disk secondarily (spondy- lodiskitis). Simple diskitis may only be found in children or result from iatrogenic procedures. The vertebral

arches are very rarely involved in an infectious process.

Inflammatory processes may reveal different appear- ances due to individual differences in the velocity of infection and the reaction of bone and soft tissue. At first there is a bacteriemia (viremia) followed by localized edema, demineralization with reactive hyperemia, and demarcation by fibrovascular tissue. Repair starts from outside. Activation of osteoclasts and transformation of fibroblasts into osteoblasts leads to new bone formation (primitive bone with a high density). Granulomatous spondylitis may show in about 30% soft tissue calcification. Finally, there is complete healing with rebuilding of trabecular and cortical bone. In some cases, this last step does not take place. In such a case, the dense calcified bone remains unchanged.

Possible complications are abscesses, which may develop within the bone or near the spine. Dead bone within the abscess in the bone is called a sequestrum.

The paraspinal abscess formation – particularly in tuberculosis – may involve surrounding soft tissue and spinal cord. In granulomatous spondylitis, several vertebral segments are typically involved. The propagation occurs preferentially in the anterior subligamentous zone (Fig. 28). In the worst case – particularly in granulomatous spondylitis – the disease may end up in severe kyphosis with eventual ankylosis (Pott’s disease) [5, 13].

While in pyogenic spondylitis the infectious process may be localized in the lower lumbar spine or thoraco- lumbar transition, the granulomatous entity involves more commonly the lower half of the thoracic and the lumbar spine.

In about 10%–20% of all cases, acute spondylitis is transformed to chronic spondylitis (by definition, if there is not complete healing after 6 months), due to de- layed diagnosis, insufficient treatment or inadequate Fig. 27.Schematic drawing of the arteries of a vertebral body: up to the age of 4 years, all arteries are interconnected. In the adult and older children the arterial connections become obliterated (dotted lines) resulting in end arteries

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host defense. It is characterized by recurrent exacerba- tions of acute disease and insufficient healing. In many cases, it is the result of granulomatous, rarely of pyogenic spondylitis.

Imaging

Early diagnosis is possible using MRI. Hyperemia and the higher metabolic turnover of bone lead to localized T2 hyperintensity (edema) (Fig. 29) with contrast enhancement on T1-weighted images (hyperemia and reactive fibrovascular tissue). The T2-hyperintensity may involve the disk. The absence of the intranuclear cleft on T2-weighted images differentiates an infected disk from a well-hydrated, healthy disk. After injection of contrast medium, the disk, adjacent vertebral bodies, and involved paraspinal/epidural soft tissues are enhanced (Fig. 30). These typical (acute) findings may change to hypointensity when calcification starts (low-intensity bands).

Three-phase bone scan has a somewhat lower accu- racy rate in acute pyogenic spondylitis in comparison to MRI. Moreover, it has a very low detail resolution: the

anatomical details cannot be differentiated. Finally, it is also very time-consuming combined with radiation, ad- ditional disadvantage. However, in unclear chronic spondylitis disease, leukocyte bone scintigraphy or antigen scintigraphy may be an excellent problem solver.

In the last years positron emission tomography (PET) with FDG (18F-fluorodeoxyglucose) has increasingly been used in suspected spondylitis. In several publications, it proved useful for differentiation of degenerative and infectious endplate abnormalities found in MRI. While PET in a high percentage (>90%) of cases was positive in infectious disease, it remained normal in all degenerative processes, even in Modic I stage [15].

The first signs of spondylitis on standard radiographs are localized demineralization and narrowing of disk space with retrolisthesis. These abnormalities are found typically near the endplates and/or anteriorly (Fig. 31). In this stage, CT (conventional or spiral CT) could already reveal erosive changes within bony structures (Fig. 32) and soft tissue swelling.

Later on, reactive sclerosis develops from the outside and is the first sign of healing on conventional radiographs (Fig. 33). Finally, after some months normaliza- tion of all bony structures can be seen. In cases of complications, a sequestrum may develop (Fig. 34). Typical- ly this is a central dense bone within a lytic lesion. The sequestrum looks more dense because the surrounding bone is porotic and the sequestrum itself may condense.

In doubtful cases, CT is the method of choice to visual- ize these abnormalities [11].

MRI is the imaging modality of choice in early diagnosis or in unclear cases during treatment. Typically, in the acute phase it shows a localized hyperintensity on T2-weighted images (edema), which may involve the disk (spondylodiscitis). Later on there is localized con- Fig. 28.Macromorphological sagittal cut of thoracic spine: infec-

tious process located anterior of and near the disk with anterior subligamentous extension

Fig. 29.Lateral T2-weighted MRI of the lumbar spine showing hyperintensity within the subchondral bone marrow, representing reactive edema in acute spondylitis

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Fig. 30A, B.Lateral T1-weighted lumbar spine.ABefore contrast medium injection and Bafter contrast medium injection.AThere is a low- intensity lesion with soft tissue involvement of L4/L5.BMarked enhancement of the complete lesion

Fig. 31.Lateral conventional radiograph of the lumbar spine showing disk space narrowing with subchondral erosion dorsally and rim calcification in subacute spondylitis

Fig. 32.Axial CT of the lumbar spine showing anterior erosions (ar- rows) with soft tissue swelling (arrowhead) in acute spondylitis

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Fig. 33.Lateral radiograph of lumbar spine: inflammatory erosive changes between L2/L3 with sclerotic margins as first signs of healing

Fig. 34.Axial CT of the lumbar spine showing several calcifications (dense bone) within a lytic lesion representing multiple sequestra in an abscess

Fig. 35A, B.MRI of tuberculous spondylitis:Aaxial and Bcoronal, both after contrast medium application.AHyperintense paraspinal soft tissue mass with multiple loculated, sharply outlined low- intensity lesions representing abscesses.BParaspinal hyperintense soft tissue masses with multiple low intensities

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trast enhancement on T1-weighted images starting from the outside. Finally, fatty marrow conversion takes places, which is also a marker of healing. Other signs of a favorable response to treatment are calcification on standard radiographs, reduction of edema and soft-tissue swelling and less enhancement after contrast medium injection.

Complications such as soft tissue and epidural abscesses are best seen with MRI or CT. Typically, a homo- geneous fluid is found centrally, surrounded by soft tissue rim or irregular thickness. After contrast medium application, a rim enhancement is demonstrated (Fig. 35).

Granulomatous (tuberculous) spondylitis reveals the same basic imaging symptoms as pyogenic spondylitis, but progresses very slowly over months with minor clinical symptoms. Soft tissue swelling (with calcification) may be very prominent, and a huge soft tissue abscess may be found (e.g., psoas abscess, epidural abscess). Typically, tuberculous spondylitis can affect several neighboring vertebral bodies.

Rare pathogens of spondylitis are fungi or parasites.

In fungal spondylitis, the imaging signs are very similar to those seen in tuberculosis. Parasitic spondylitis usu- ally shows very typical findings (e.g., Echinococcus cyst).

Blastoma and granulomatous spondylitis may present a differential diagnostic problem. Characteristi- cally, blastomas (except myeloma and chordoma) do not involve the disk, while spondylitis almost always does (Fig. 36).

Early cases of spondylitis and stage I degeneration (pseudoinflammation) may be another differential diagnostic problem. Typically in spondylitis, the disk is edematous (hyperintense on T2-weighted images), while in degeneration there are low intensities on T1- and T2-weighted images, or even gas. The disk space is narrowed.

Eventually FDG-PET could serve as a problem solver, as described above.

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Fig. 36.Lateral T2-weighted MRI of the cervical spine: huge soft tissue mass at C7 with paraspinal and epidural extension. The disks seem to be preserved. Histology: lymphoma